Interstitial Cystitis (IC) is a disease of unknown origin that is recognized primarily by its symptomatic presentation. These symptoms include suprapubic pain, frequency, nocturia and urgency. The etiology of IC is unknown. Numerous causes have been hypothesized including infection, vascular and/or lymphatic obstruction, inflammation, neurogenic bladders, endocrinologic disorders, autoimmunity, loss of the mucopolysaccharide layer, and the presence of toxic substances in the urine. There is no strong evidence to support a role for any of the above in the induction of IC. One of the reasons for the paucity of knowledge concerning this disease is the absence of an animal model. We have developed a model of experimental autoimmune cystitis (EAC) that appears to exhibit biological equivalency with IC in that pathological and physiological parameters are similar. Our preliminary studies indicate that the EAC model is similar to clinical IC in the character of the inflammatory response and the expression of physiological parameters such as increased vascularity, reduced bladder capacity and the development of glomerulations after bladder distention. We propose to use this model to develop a better understanding of the inflammatory process associated with IC. We will characterize the model with regard to mouse strain susceptibility, modulating factors that influence the induction of the inflammatory process and physiological correlations with clinical IC. We will also purify the inducing antigens and characterize the immunlogical mechanisms responsible for the induction of the disease process.